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Aim Patients and Methods Results Conclusion This study aims to investigate the role of recombinant human type III collagen (RHC3) in preventing abdominal adhesion.The amino acid sequence was analysed to determine the content of GPP fragments. RHC3 was co‐cultured with macrophages, and the phenotypic classification of macrophages was based on immunofluorescence detection of inducible nitric oxide synthase for M1 macrophages and arginase 1 for M2 macrophages. This approach was used to assess the impact of RHC3 on promoting M2 polarisation. Levels of inflammatory factor levels, including interleukin 1‐beta (IL‐1β), tumour necrosis factor‐alpha (TNF‐α), and IL‐10, were quantified using enzyme‐linked immunosorbent assay to evaluate the improvement in inflammatory response. The capability of RHC3 to prevent abdominal adhesions was assessed by rinsing the abdominal cavity in an animal model.RHC3 contains GPP fragments that account for over 5% of its amino acid sequence. Cell studies indicated that RHC3 induced M2 polarisation in macrophages, significantly reduced levels of pro‐inflammatory factors (IL‐1β and TNF‐α), and significantly increased levels of the anti‐inflammatory factor IL‐10. Similarly, animal studies demonstrated a significant reduction in abdominal adhesion scores.These results suggest that RHC3 exhibits notable inflammation‐ameliorating activity and effectively prevents abdominal adhesions when used as a lavage solution. [ABSTRACT FROM AUTHOR]

Wounds are in a stressed state, which precludes healing. Trehalose is a stress metabolite that protects cells under stress. Here, we explored whether trehalose reduces stress-induced wound tissue damage. A stress model was prepared by exposing human keratinocytes to hydrogen peroxide (H 2 O 2), followed by trehalose treatment. Trehalose effects on expression of the autophagy-related proteins ATG5 and ATG7 and cell proliferation and migration were evaluated. For in vivo verification, a wound model was established in Sprague–Dawley rats, to measure the effects of trehalose wound-healing rate and reactive oxygen species (ROS) content. Histological changes during wound healing and trehalose's effects on ATG5 and ATG7 expression, necrosis, and apoptosis were examined·H 2 O 2 stress increased ATG5 and ATG7 expression in vitro , but this was insufficient to prevent stress-induced damage. Trehalose further increased ATG5/ATG7 levels, which restored proliferation and increased migration by depolymerizing the cytoskeleton. However, trehalose did not exert these effects after ATG5 and ATG7 knockout. In vivo, the ROS content was higher in the wound tissue than in normal skin. Trehalose increased ATG5/ATG7 expression in wound tissue keratinocytes, reduced necrosis, depolymerized the cytoskeleton, and promoted cell migration, thereby promoting wound healing. • Trehalose increased the concentrations of ATG5 and ATG7 in HaCat cells. • The increased concentrations of ATG5 and ATG7 promoted proliferation and migration • Trehalose-mediated protection was lost after ATG5/ATG7 knockout. • Trehalose enhanced wound healing in a rat model [ABSTRACT FROM AUTHOR]

Current wound scaffold dressing constructs can facilitate wound healing but do not exhibit antibacterial activity, resulting in high infection rates. We aimed to endow wound scaffold dressing with anti‐infective ability by polyhexamethylenebiguanide (PHMB). We prepared PHMB hydrogel at varying concentrations (0.25%, 0.5%, 1%, 2%) and assessed release and cytotoxicity. PHMB hydrogel was added to the wound scaffold dressing to generate a PHMB hydrogel‐modified wound scaffold dressing. Wound healing and infection prevention were evaluated using a full‐thickness skin defect model in rats. In vitro, the hydrogel PHMB release time positively correlated with PHMB concentration, with 1% allowing sufficiently long release time to encompass the high‐incidence period (3‐5 days) of infection following wound scaffold dressing implantation. Implantation of 1% PHMB hydrogel into the skin did not cause adverse responses. in vitro cytotoxicity assays showed the PHMB hydrogel‐modified wound scaffold dressing did not significantly affect proliferation of fibroblasts or vascular endothelial cells, 99.90% vs 99.84% for fibroblasts and 100.21% vs 99.28% for vascular endothelial cells at 21 days. Transplantation of PHMB hydrogel‐modified wound scaffold dressing/unmodified wound scaffold dressing on the non‐infected wounds of rats yielded no significant difference in relative vascularization rate, 47.40 vs 50.87 per view at 21 days, whereas bacterial content of the wound tissue in the PHMB hydrogel‐modified wound scaffold dressing group was significantly lower than the unmodified wound scaffold dressing group, (1.80 ± 0.35) × 103 vs (9.34 ± 0.45) × 103 at 14 days. Prevalence of persistent wound infection in the rats receiving PHMB hydrogel‐modified wound scaffold dressing transplantation onto infected wounds was significantly lower than the unmodified wound scaffold dressing group, 30% vs 100%. PHMB hydrogel‐modified wound scaffold dressing exhibited suitable antibacterial ability, and its biological activity did not significantly differ from that of the unmodified wound scaffold dressing, thereby allowing it to effectively prevent infection following wound scaffold dressing implantation. [ABSTRACT FROM AUTHOR]